Middle Cerebral Artery Flow Velocity and Cerebral Oxygenation during Abdominal Aortic Surgery

Abstract

Cerebral perfusion was evaluated in twelve patients undergoing elective infra-renal abdominal aortic aneurysmectomy by transcranial Doppler ultrasonography-determined middle cerebral artery mean flow velocity, near-infrared spectroscopy-assessed cerebral oxygen saturation and systemic haemodynamic variables. The middle cerebral artery mean flow velocity and cerebral oxygen saturation decreased during cross-clamping of the aorta, and both increased upon declamping of the aorta with the oxygen saturation change lagging behind the change in the flow velocity. The changes in cerebral flow velocity and oxygen saturation paralleled the deviations in cardiac output and end-tidal carbon dioxide tension.

Near-infrared spectroscopy assessed cerebral oxygenation during open abdominal aortic aneurysm repair: relation to end-tidal CO2 tension

“…In support, S c O 2 was related to EtCO 2 and in the patient who demonstrated a marked increase in S c O 2 upon reperfusion of the lower body, ventilation was not increased. According to the anesthetic charts reviewed the present patients were exposed to less marked changes in cerebral oxygenation than those studied by Liu et al [17] for whom no ventilatory adjustments were made.…”

“…1). Peak inspiratory pressure (16 cm H 2 O; [16][17] and positive end-expiratory pressure (5 cm H 2 O) were kept stable. Conversely, during reperfusion of the aorta S c O 2 increased 2 % (-1 to 4; P \ 0.001) as EtCO 2 became 0.5 kPa (0.1-1; P \ 0.001) elevated although ventilation was increased by 1.8 l min -1 (0.9-2.7; P \ 0.001) with an increase peak inspiratory pressure from 16 to 17 cm H 2 O (P = 0.003).…”

“…Thus, the need for CO 2 elimination is reduced and that affects CBF if ventilation is not reduced [17,18]. Liu et al [17] found that such unintended hyperventilation appears with a 13 % reduction in EtCO 2 and a consequent reduction in MCAv mean by 12 % and in S c O 2 by 4 % relative to the dissection phase.…”

“…For patients undergoing open abdominal aortic aneurysm repair, cross clamping of the aorta below the renal vessels reduces cardiac output (CO) and end-tidal CO 2 (EtCO 2 ) decreases if ventilation is not lowered to compensate for attenuated need of CO 2 elimination and, accordingly, S c O 2 may become affected [17]. Conversely, with reperfusion of the lower body, vasodilatory substances including CO 2 are liberated to the circulation and provoke cerebral hyperperfusion as illustrated by a *50 % increase in CBF [17,18] that can lead to neurological complication and even death [19].…”

“…Conversely, with reperfusion of the lower body, vasodilatory substances including CO 2 are liberated to the circulation and provoke cerebral hyperperfusion as illustrated by a *50 % increase in CBF [17,18] that can lead to neurological complication and even death [19]. Following the observations by Liu et al [17] the department intend to maintain S c O 2 throughout open AAA repair by adjusting ventilation upon clamping and reperfusion of the aorta and this retrospective study evaluates, for forty-four patients, how well that ventilatory strategy is followed. Thus, we evaluated to what extent S c O 2 was kept within reasonable limits (±15 %) and whether eventual changes in S c O 2 during open AAA repair were related to those in EtCO 2 and thus ventilation.…”